[Ethical issues and living unrelated donor kidney transplantation]

During the past decades, the number of altruistic living unrelated kidney donations has substantially increased in developed countries. However, the altruistic supply of transplantable kidneys has remained much less than the demand. As a result, severe kidney shortage has been associated with increasing number of patient deaths and increasing number of commercial transplants and transplant tourism. Studies have shown that there is still a need for living kidney donation because even all potential brain-dead donors cannot supply the escalating need for kidneys. The use of living unrelated kidney donors should be morally and ethically justified and should be compatible with ethical principles. Many experts believe that increasing number of patient deaths and commercial transplants will continue to happen if kidney donation system remains merely altruistic. While some transplant professionals support a paid and regulated system to eliminate kidney shortage, others argue that it will be destructive. Iran has a 20-year experience with a compensated and regulated living unrelated kidney donation program. This transplantation model was adopted in 1988, and successfully eliminated kidney transplant waiting list by the end of 1999. Currently, more than 50% of patients with end-stage kidney disease in Iran are living with a functioning graft. This Iranian transplantation model has many ethical successes. However, because it has not been well regulated by transplant ethicists, some ethical shortcomings have remained. Unfortunately, due to lack of interest and expertise in health authorities, the number of serious ethical failures is also increasing in this transplantation model

Estimation of glomerular filtration rate with creatinine-based versus cystatin C-based equations in kidney transplant recipients

Serum cystatin C is more sensitive for glomerular filtration rate [GFR] measurement, but it is not available for clinical use in all laboratories. Regarding the importance of accurate estimation of GFR in kidney transplant recipients, we compared cystatin C-based equations with creatinine-based formulas to estimate GFR as precisely and simply as possible in kidney transplant recipients. Seventy living donor kidney transplant recipients with stable kidney function were enrolled in our study. The patients' GFRs were estimated by 3 creatinine-based equations [the modification of diet in renal disease [MDRD], abbreviated MDRD, and Cockcroft-Gault] and 5 cystatin C-based equations [Filler, Le Bricon, Rule, Hoek, and Larsson], and the results were analyzed. The mean age of the recipients was 38.7 +/- 13.4 years. The mean GFRs were 67.1 +/- 25.9 mL/min/1.73 m[2], by the Cockcroft-Gault; 61.0 +/- 17.7 mL/min/1.73 m[2], by the abbreviated MDRD; and 60.0 +/- 18.6 mL/min/1.73 m[2], by the MDRD formulas. Cystatin C-based GFR estimations were 43.6 +/- 16.2 mL/min/1.73 m[2], 44.0 +/- 13.2 mL/min/1.73 m[2], 33.8 +/- 14.1 mL/min/1.73 m[2], 35.6 +/- 13.7 mL/min/1.73 m[2], and 36.9 +/- 13.6 mL/min/1.73 m[2] by the Filler, Le Bricon, Larsson, Rule, and Hoek equations, respectively. The estimates by creatinine-based and cystatin C-based equations were significantly different and the MDRD estimate was the closest to the cystatin C-based GFRs. Our findings revealed the MDRD equation could be provide a closer estimate of GFR to the cystatin C-based equations than other creatinine-based GFR calculations in kidney transplant recipients

High frequency of clinically significant infections and cytomegalovirus disease in kidney transplant recipients with serum mannose-binding lectin deficiency

Mannose-binding lectin [MBL] constitutes defense against infections when adaptive immune response is compromised. Elevation in serum MBL levels has been shown in patients with kidney failure. We compared serum MBL levels before and after kidney transplant and evaluated association of MBL deficiency with infectious complications in kidney transplant recipients. This study was performed in 71 kidney transplant recipients and 48 healthy controls. In 36 recipients [group 1], serum MBL levels were tested before and on days 7 and 14 after transplantation. They were followed up for 6 months. In 35 recipients [group 2], serum MBL was measured during their posttransplant follow-up visits. In both groups, frequencies of clinically significant infections and acute rejection were compared between those with low MBL [< 500 ng/mL] and normal/high MBL [< 500 ng/mL]. Serum MBL levels [1744 +/- 905 ng/mL] were not higher in group 1 before transplantation than in controls. One and 2 weeks after transplantation, MBL levels decreased to 1699 +/- 1030 ng/mL and 1562 +/- 1020 ng/mL, respectively. Five patients who had low serum MBL levels experienced more frequent episodes of infections [P = .008] and CMV disease [P < .001]. Ten patients in group 2 with low MBL levels had more frequent episodes of CMV disease [P = .01]. These findings suggest a potential role for MBL in defense against developing posttransplant CMV disease and that low serum MBL levels in kidney transplant recipients be considered an indicator of the need for CMV prophylaxis

Posttransplant diabetes mellitus in kidney allograft recipients at Shaheed Hasheminejad Hospital

Our aim was to evaluate the frequency and risk factors of posttransplant diabetes mellitus [PTDM] at our kidney transplant center, and to compare graft and patient outcomes between the kidney recipients with and without PTDM. We studied 203 kidney transplant recipients with a negative history of diabetes mellitus before transplantation. We examined them for PTDM and made diagnosis on the basis of the American Diabetes Association criteria. Measurements of plasma glucose were carried out from 3 months to 24 months after transplantation. All data including recipient and donor demographics, cause of end-stage renal disease, cytomegalovirus and hepatitis C virus antibody tests, and patient and graft outcomes were assessed in relation to PTDM. High fasting plasma glucose was seen in 24 [11.8%], 19 [9.4%], 16 [7.9%], and 13 [6.4%] patients at 3, 6, 12, and 24 posttransplant months, respectively. Moreover, impaired glucose tolerance was seen in 17 [8.4%], 16 [7.9%], 17 [8.4%], and 19 [9.4%] patients at the corresponding times, respectively. Accordingly, 39 patients [19.2%] were diagnosed to have PTDM. The mean age of the kidney recipients with PTDM was 46.5 +/- 12.3 years as compared to 38.6 +/- 13.4 years in nondiabetic kidney recipients [P = .02]. The 5-year patient and graft survival rates were not significantly different between the kidney recipients with and without PTDM. This study showed that PTDM is a common metabolic disorder in our kidney transplant patients. We recommend a less diabetogenic immunosuppressive protocol, especially for our older recipients